Insights into the effects of contraction dyssynchrony on global left ventricular mechano-energetic function.
Insights into the effects of contraction dyssynchrony on global left ventricular mechano-energetic function.
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DOI：
10.1111/j.1540-8159.2008.02206.x
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发表时间：
2009-02
期刊：
影响因子：
--
通讯作者：
Shroff SG
中科院分区：
文献类型：
--
作者：
Johnson L;Simon MA;Pinsky MR;Shroff SG
不同步性对整体左心室(LV)力学的影响已经有了很好的文献记载，然而，它对LV能量学的影响却较少受到关注。在起搏诱导的急性不同步模型中，评估左心室收缩不同步对整体左心室机械能功能的影响。采用灌流离体兔心脏标本(n=11)，记录右房(RA)起搏(对照组)和右室和右室流出道(RVOT)同时起搏(不同步)下等容收缩的LV压、冠脉流量和动静脉氧含量差。用收缩末期压力-容量关系(ESPVR)定量评价左心室机械功能。心肌耗氧量-压力-容积面积(MVO2-PVA)关系量化左心室能量功能。根据Ra起搏的MVO2-PVA关系计算MVO2RVOT的内部PVA。因此，损失的PVA(内部PVA−PVARVOT)代表在全球水平上看不到的机械能。与RA起搏相比，RVOT起搏降低了LV力学，表现为ESPVR右移(即Vd从0.58±0.10增加到0.67±0.10毫升，P<0.05)。尽管机械性能降低，但右室流出道起搏与更大的MVO2相关，使MVO2-PVA关系截距从0.025±0.003增加到0.029±0.003毫升·O2/次/100gLV(P<0.05)。MVO2过高(即MVO2RVOTMVO2RA)与−丢失显著相关(R2=0.54P&0.001)。解释观察到的MVO2不同步增加的一个潜在机制可能是，在全球水平测量的PVA低估了细胞水平的内部PVA，这很可能是MVO2的真正决定因素。
The effects of dyssynchrony on global left ventricular (LV) mechanics have been well documented; however, its impact on LV energetics has received less attention. To assess the effects of LV contraction dyssynchrony on global LV mechano-energetic function in a pacing-induced acute model of dyssynchrony. Using blood-perfused isolated rabbit heart preparations (n = 11), LV pressure, coronary flow, and arteriovenous oxygen content difference were recorded for isovolumic contractions under right atrial (RA) pacing (control) and simultaneous RA and right ventricular outflow tract (RVOT) pacing (dyssynchrony). LV mechanical function was quantified by the end-systolic pressure-volume relationship (ESPVR). Myocardial oxygen consumption-pressure-volume area (MVO2-PVA) relationship quantified LV energetic function. Internal PVA for MVO2RVOT was calculated based on the MVO2-PVA relationship for RA pacing. Thus, lost PVA (internal PVA− PVARVOT) represents the mechanical energy not observable at the global level. Compared to RA pacing, RVOT pacing depressed LV mechanics as indicated by a rightward shift of ESPVR (i.e., increase in Vd from 0.58 ± 0.10 to 0.67 ± 0.10 mL, P < 0.05). Despite depressed mechanics, RVOT pacing was associated with greater MVO2 such that the MVO2-PVA relationship intercept was markedly increased from 0.025 ± 0.003 to 0.029 ± 0.003 mL•O2/beat/100gLV (P < 0.05). Excess MVO2 (i.e., MVO2RVOT − MVO2RA) significantly correlated with lost PVA (R2 = 0.54, P < 0.001). A potential mechanism explaining the observed increase in MVO2 with dyssynchrony may be that the measured PVA at the global level underestimates the internal PVA at the cellular level, which is likely to be the true determinant of MVO2.
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影响因子：
24
作者：
Bader, H;Garrigue, S;Roudaut, R
通讯作者：
Roudaut, R
影响因子：
--
作者：
SUGA, H;HAYASHI, T;SHIRAHATA, M
通讯作者：
SHIRAHATA, M
影响因子：
--
作者：
PRINZEN, FW;AUGUSTIJN, CH;RENEMAN, RS
通讯作者：
RENEMAN, RS
影响因子：
20.1
作者：
SUGA, H;SAGAWA, K
通讯作者：
SAGAWA, K
影响因子：
20.1
作者：
CAMPBELL, KB;SHROFF, SG;KIRKPATRICK, RD
通讯作者：
KIRKPATRICK, RD